Reflux of upper intestinal content, in general, and of bile acids, in particular, has been implicated in the development of acute and chronic gastric mucosal disease, specifically, acute post-traumatic hemorrhagic gastritis, type I benign gastric ulcer, and post-operative alkaline reflux gastritis. The present request proposes to examine, in the experimental laboratory, the pathophysiology of these disease entities by investigating (1) the relationship of surface epithelial cells to mucosal integrity, (2) the influence of bile acids on active Na ion transport and tissue water distribution in gastric mucosa, (3) the effect of systemic prostaglandins in providing "cytoprotection" to bile acid treated mucosa, (4) the influence of lysolecithin both alone and in combination with the bile acids in gastric mucosa, and (6) the mechanisms of delayed gastric emptying following Roux-Y diversion of upper intestinal content. In a related clinical study of post-operative alkaline reflux gastritis, the present request proposes to define that syndrome more precisely by quantitating differences between symptomatic and asymptomatic post-gastrectomy patients with respect to (1) the magnitude of enterogastric reflux determined by radionuclide scanning and net bile acid reflux, (2) reflux of specific bile acid fractions, of lysolecithin, and of pancreatic phospholipase A-2, (3) enteric concentrations of the same factors, (4) the symptomatic response to exogenously administered bile acids and reflux content, and (5), as before, the relationship of reflux to histologic gastritis.